Potential mechanisms of non-suicidal self-injury (NSSI) in major depressive disorder: a systematic review.

Background: Non-suicidal self-injury (NSSI) is a frequent and prominent phenomenon in major depressive disorder (MDD). Even though its prevalence and risk factors are relatively well understood, the potential mechanisms of NSSI in MDD remain elusive. Aims: To review present evidence related to the potential mechanisms of NSSI in MDD. Methods: According to Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines, articles for this systematic review were searched on Medline (through PubMed), Embase (through Elsevier), PsycINFO (through OVID) and Web of Science databases for English articles, as well as China National Knowledge Infrastructure (CNKI), SinoMed, Wanfang Data, and the Chongqing VIP Chinese Science and Technology Periodical (VIP) Databases for Chinese articles published from the date of inception to 2 August 2022. Two researchers (BW, HZ) independently screened studies based on inclusion and exclusion criteria and assessed their quality. Results: A total of 25 157 studies were searched. Only 25 of them were ultimately included, containing 3336 subjects (1535 patients with MDD and NSSI, 1403 patients with MDD without NSSI and 398 HCs). Included studies were divided into 6 categories: psychosocial factors (11 studies), neuroimaging (8 studies), stress and hypothalamic-pituitary-adrenal (HPA) axis (2 studies), pain perception (1 study), electroencephalogram (EEG) (2 studies) and epigenetics (1 study). Conclusions: This systematic review indicates that patients with MDD and NSSI might have specific psychosocial factors, aberrant brain functions and neurochemical metabolisms, HPA axis dysfunctions, abnormal pain perceptions and epigenetic alterations.

Differences in cognitive functions of atypical and non-atypical depression based on propensity score matching.

BACKGROUND: Clinical and etiological heterogeneity have hindered our understanding of depression, thus driving the studies of major depressive disorder (MDD) subtypes. Atypical depression (AD) is a subtype of MDD with atypical features. Cognitive impairment is one of the factors that contribute to the suffering of patients with MDD. Therefore, this study investigated the characteristics and differences in cognitive functioning of AD and non-atypical depression (non-AD) using the MATRICS Consensus Cognitive Battery (MCCB). METHODS: A total of 101 patients with AD and 252 patients with non-AD were assessed with the MCCB and clinical scales. Propensity score matching (PSM) was used to balance confounders between groups. After PSM, between-group differences were compared for cognitive and clinical variables. In addition, multiple linear regression analyses were performed to explore the effects of cognitive and clinical variables on the quality of life. RESULTS: The AD group scored significantly lower in attention/vigilance and social cognition in all cognitive domains than the non-AD group. Attention/vigilance and social cognition were significant positive predictors of quality of life, whereas atypical symptoms and depressive severity were significant negative predictors. CONCLUSIONS: This study suggests significant differences in cognitive functions between the AD and non-AD subtypes. Atypical symptoms and impaired cognition have a negative impact on patients' quality of life. Attention/vigilance and social cognition are worse in AD than non-AD, which the atypical features of patients with AD may explain. The pathological mechanisms and treatment strategies of AD should be further explored in the future to promote individualized treatment strategies.

Efficient Registration for Human Surfaces via Isometric Regularization on Embedded Deformation.

3D registration is a fundamental step to obtain the correspondences between surfaces. Traditional mesh alignment methods tackle this problem through non-rigid deformation, mostly accomplished by applying ICP-based (Iterative Closest Point) optimization. The embedded deformation method is proposed for the purpose of acceleration, which enables various real-time applications. However, it regularizes on an underlying simplified structure, which could be problematic for intricate cases when the simplified graph doesn't fully represent the surface attributes. Moreover, without elaborate parameter-tuning, deformation usually performs suboptimally, leading to slow convergence or a local minimum if all regions on the surface are assumed to share the same rigidity during the optimization. In this article, we propose a novel solution that decouples regularization from the underlying deformation model by explicitly managing the rigidity of vertex clusters. We further design an efficient two-step solution that alternates between isometric deformation and embedded deformation with cluster-based regularization. Our method can easily support region-adaptive regularization with cluster refinement and execute efficiently. Extensive experiments demonstrate the effectiveness of our approach for mesh alignment tasks even under large-scale deformation and imperfect data. Our method outperforms state-of-the-art methods both numerically and visually.

Natural Xanthone α-Mangostin Inhibits LPS-Induced Microglial Inflammatory Responses and Memory Impairment by Blocking the TAK1/NF-κB Signaling Pathway.

SCOPE: The effect of α-mangostin (α-M), a polyphenolic xanthone isolated from mangostin, on lipopolysaccharide (LPS)-induced microglial activation and memory impairment is explored. The possible underlying mechanisms are also investigated. METHODS AND RESULTS: Cytokine production and activation of transforming growth factor activated kinase-1 (TAK1) and nuclear factor-κB (NF-κB) are detected by enzyme-linked immunosorbent assay (ELISA) or Western blot. Microglial migration and phagocytosis are evaluated with scratch wound-healing assay and phagocytosis of fluorescent latex beads, respectively. Learning and memory abilities of mice are evaluated with the Morris water maze test. The nanomolar (100-500 nm) α-M suppresses LPS-induced pro-inflammatory cytokine production and inducible nitric oxide synthase (iNOS) expression in microglia. It also inhibits LPS-induced microglial migration and phagocytosis. α-M rescues LPS-caused, microglia-mediated neuronal dendritic damage. Moreover, α-M represses LPS-induced toll-like receptor 4 (TLR4) expression and activation of TAK1 and NF-κB. In a mouse neuroinflammation model, α-M (50 mg kg-1 day-1 ) shows obvious anti-neuroinflammatory, neuroprotective, and memory-improving effects in vivo. CONCLUSION: α-M inhibits microglia-mediated neuroinflammation and prevents neurotoxicity and memory impairment from inflammatory damage. These results indicate that α-M has great potential to be used as a nutritional preventive strategy for neuroinflammation-related neurodegenerative disorders such as Alzheimer's disease.

A multifunctional bis-(-)-nor-meptazinol-oxalamide hybrid with metal-chelating property ameliorates Cu(II)-induced spatial learning and memory deficits via preventing neuroinflammation and oxido-nitrosative stress in mice.

Excess copper exposure is a risk factor of neurodegeneration related to Alzheimer's disease (AD). Evidence indicates that, besides promoting amyloid ß aggregation, activation of neuroinflammation and oxido-nitrosative stress (two key pathophysiological processes of AD) may also play important roles in Cu(II)-induced neuronal injury. Therefore, the copper-chelating strategy has gained attention in search for new anti-AD drugs. We previously reported a novel multifunctional compound N1,N2-bis(3-(S)-meptazinol-propyl) oxalamide (ZLA), a bis-(-)-nor-meptazinol-oxalamide hybrid with properties of dual binding site acetylcholinesterase (AChE) inhibition and Cu(II)/Zn(II) chelation. The present study was aimed to explore its effect on cognitive deficits caused by intrahippocampal injection of Cu(II) in mice. Results showed that ZLA (2, 5 mg/kg; i.p.) treatment significantly ameliorated the Cu(II)-induced impairment of hippocampus-dependent learning and memory, whereas rivastigmine, an AChE inhibitor showing a similar potency of enzyme inhibition to ZLA, had no obvious effect. Immunohistochemical and Western blot analyses revealed that ZLA attenuated the decrease in hippocampal expression of microtubule-associated protein 2 (MAP2, a dendritic marker) in Cu(II)-challenged mice. Further analysis showed that ZLA suppressed the Cu(II)-evoked microglial activation. Moreover, it inhibited the Cu(II)-evoked production of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1ß and expression of inducible nitric oxide synthase in the hippocampus. The Cu(II)-induced oxidative and nitrosative stress in the hippocampus was also attenuated after ZLA treatment. Collectively, these results suggest that ZLA ameliorates the Cu(II)-caused cognitive deficits. Inhibition of neuroinflammation and oxido-nitrosative stress, and thus ameliorating neuronal injury, may be the potential mechanism for the anti-amnesic effect of ZLA.